About one month before birth, the testis enters the inguinal canal through the internal ring and after birth enters the scrotum. The peritoneum enters the scrotum with the testis and forms the peritoneal sheath, which should be occluded when normal, and the sheath may form a hernia if it is open or incompletely occluded. Anatomical structural defects: the inguinal region is an area without muscle protection and is passed by the spermatic cord or the round ligament of the uterus, where the inguinal canal with a spiral step structure is formed. The internal ring is an important weak point in the lower abdominal wall, and a hiatal hernia is formed through this opening when the visceral pressure is high enough to enter the inguinal canal. Loss of physiological defense of the inguinal canal: The anatomical defects of the inguinal canal area are compensated and strengthened by physiological defenses such as the sphincter-like action of the contraction of the internal oblique and transversus abdominis muscles and the clamp-closing apparatus function of the transversus abdominis tendon arch. Elevated intra-abdominal pressure plays an important role in the development and progression of inguinal hernias: when the body is upright, the pressure on the abdominal wall in the inguinal region is three times higher than usual. Under certain physiological or pathological conditions, such as labor, obesity, cough, constipation, prostate hypertrophy, ascites, etc., when intra-abdominal pressure is continuously elevated, the physiological anatomical structure and physiological defense functions of the inguinal region are destroyed, such as fascia, ligaments and muscles are stretched, degeneration occurs and become thinner and looser, the annular fissure gradually widens, and inguinal hernia naturally forms. Collagen metabolism and hernia: The formation of hernia is related to the decrease of collagen synthesis and increase of collagen breakdown. The increase of elastolytic enzyme activity in blood and the decrease of inhibited proteolytic enzyme (α1-antitrypsin) increase collagen breakdown. Smoking: Smoking can cause a decrease in circulating inhibited proteolytic enzymes, while proteolytic enzymes (including elastase) are produced in the lungs to enter the blood circulation, causing the destruction of collagen and elastin in the organism and the destruction of the transversus abdominis fascia and transversus abdominis tendon membrane layer in the inguinal region, causing the creation of hernias. In conclusion, congenital anatomical abnormalities and acquired factors causing weakness or defect of the abdominal wall and increased intra-abdominal pressure are the etiology.